Not all models are explanatory. Some models are data summaries. Some models sketch explanations but leave crucial details unspecified or hidden behind filler terms. Some models are used to conjecture a how-possibly explanation without regard to whether it is a how-actually explanation. I use the Hodgkin and Huxley model of the action potential to illustrate these ways that models can be useful without explaining. I then use the subsequent development of the explanation of the action potential to show what is (...) required of an adequate mechanistic model. Mechanistic models are explanatory. (shrink)

We argue that neuroeconomics should be a mechanistic science. We defend this view as preferable both to a revolutionary perspective, according to which classical economics is eliminated in favour of neuroeconomics, and to a classical economic perspective, according to which economics is insulated from facts about psychology and neuroscience. We argue that, like other mechanistic sciences, neuroeconomics will earn its keep to the extent that it either reconfigures how economists think about decision-making or how neuroscientists think about brain mechanisms underlying (...) behaviour. We discuss some ways that the search for mechanisms can bring about such top-down and bottom-up revision, and we consider some examples from the recent neuroeconomics literature of how varieties of progress of this sort might be achieved. (shrink)

Defining and identifying causal intervention effects for transmissible infectious disease outcomes is challenging because a treatment – such as a vaccine – given to one individual may affect the infection outcomes of others. Epidemiologists have proposed causal estimands to quantify effects of interventions under contagion using a two-person partnership model. These simple conceptual models have helped researchers develop causal estimands relevant to clinical evaluation of vaccine effects. However, many of these partnership models are formulated under structural assumptions that preclude realistic (...) infectious disease transmission dynamics, limiting their conceptual usefulness in defining and identifying causal treatment effects in empirical intervention trials. In this paper, we propose causal intervention effects in two-person partnerships under arbitrary infectious disease transmission dynamics, and give nonparametric identification results showing how effects can be estimated in empirical trials using time-to-infection or binary outcome data. The key insight is that contagion is a causal phenomenon that induces conditional independencies on infection outcomes that can be exploited for the identification of clinically meaningful causal estimands. These new estimands are compared to existing quantities, and results are illustrated using a realistic simulation of an HIV vaccine trial. (shrink)

The dominant neuroscientific theory of spatial memory is, like many theories in neuroscience, a multilevel description of a mechanism. The theory links the activities of molecules, cells, brain regions, and whole organisms into an integrated sketch of an explanation for the ability of organisms to navigate novel environments. Here I develop a taxonomy of interlevel experimental strategies for integrating the levels in such multilevel mechanisms. These experimental strategies include activation strategies, interference strategies, and additive strategies. These strategies are mutually reinforcing, (...) providing a kind of interlevel and intratheoretic robustness that has not previously been recognized. (shrink)

The pivotal problem of comorbidity research lies in the psychometric foundation it rests on, that is, latent variable theory, in which a mental disorder is viewed as a latent variable that causes a constellation of symptoms. From this perspective, comorbidity is a (bi)directional relationship between multiple latent variables. We argue that such a latent variable perspective encounters serious problems in the study of comorbidity, and offer a radically different conceptualization in terms of a network approach, where comorbidity is hypothesized to (...) arise from direct relations between symptoms of multiple disorders. We propose a method to visualize comorbidity networks and, based on an empirical network for major depression and generalized anxiety, we argue that this approach generates realistic hypotheses about pathways to comorbidity, overlapping symptoms, and diagnostic boundaries, that are not naturally accommodated by latent variable models: Some pathways to comorbidity through the symptom space are more likely than others; those pathways generally have the same direction (i.e., from symptoms of one disorder to symptoms of the other); overlapping symptoms play an important role in comorbidity; and boundaries between diagnostic categories are necessarily fuzzy. (shrink)

This paper proposes a revision of our understanding of causation that is designed to address what Hartry Field has suggested is the central problem in the metaphysics of causation today: reconciling Bertrand Russell’s arguments that the concept of causation can play no role in the advanced sciences with Nancy Cartwright’s arguments that causal concepts are essential to a scientific understanding of the world. The paper shows that Russell’s main argument is, ironically, very similar to an argument that Cartwright has put (...) forward against the truth of universal laws of nature. The paper uses this insight to develop an account of causation that does justice to traditional views yet avoids the arguments of Russell. (shrink)

Belief polarization is said to occur when two people respond to the same evidence by updating their beliefs in opposite directions. This response is considered to be “irrational” because it involves contrary updating, a form of belief updating that appears to violate normatively optimal responding, as for example dictated by Bayes' theorem. In light of much evidence that people are capable of normatively optimal behavior, belief polarization presents a puzzling exception. We show that Bayesian networks, or Bayes nets, can simulate (...) rational belief updating. When fit to experimental data, Bayes nets can help identify the factors that contribute to polarization. We present a study into belief updating concerning the reality of climate change in response to information about the scientific consensus on anthropogenic global warming. The study used representative samples of Australian and U.S. participants. Among Australians, consensus information partially neutralized the influence of worldview, with free-market supporters showing a greater increase in acceptance of human-caused global warming relative to free-market opponents. In contrast, while consensus information overall had a positive effect on perceived consensus among U.S. participants, there was a reduction in perceived consensus and acceptance of human-caused global warming for strong supporters of unregulated free markets. Fitting a Bayes net model to the data indicated that under a Bayesian framework, free-market support is a significant driver of beliefs about climate change and trust in climate scientists. Further, active distrust of climate scientists among a small number of U.S. conservatives drives contrary updating in response to consensus information among this particular group. (shrink)

Life-science phenomena are often explained by specifying the mechanisms that bring them about. The new mechanistic philosophers have done much to substantiate this claim and to provide us with a better understanding of what mechanisms are and how they explain. Although there is disagreement among current mechanists on various issues, they share a common core position and a seeming commitment to some form of scientific realism. But is such a commitment necessary? Is it the best way to go about mechanistic (...) explanation? In this article, we propose an alternative antirealist account that also fits explanatory practice in the life sciences. We pay special attention to mechanistic models, i.e. scientific models that involve a mechanism, and to the role of coherence considerations in building such models. To illustrate our points, we consider the mechanism for the action potential. 1 Introduction2 Some Core Features of Mechanistic Explanation3 Scientific Realism and Mechanistic Explanation4 Antirealist Mechanistic Explanation: The Case of the Action Potential5 Some Outstanding Issues for the Antirealist Mechanist6 Two Problems for the Realist Mechanist7 Conclusions. (shrink)

Explanation is a central concept in human psychology. Drawing upon philosophical theories of explanation, psychologists have recently begun to examine the relationship between explanation, probability and causality. Our study advances this growing literature in the intersection of psychology and philosophy of science by systematically investigating how judgments of explanatory power are affected by the prior credibility of a potential explanation, the causal framing used to describe the explanation, the generalizability of the explanation, and its statistical relevance for the evidence. Collectively, (...) the results of our five experiments support the hypothesis that the prior credibility of a causal explanation plays a central role in explanatory reasoning: first, because of the presence of strong main effects on judgments of explanatory power, and second, because of the gate-keeping role it has for other factors. Highly credible explanations were not susceptible to causal framing effects. Instead, highly credible hypotheses were sensitive to the effects of factors which are usually considered relevant from a normative point of view: the generalizability of an explanation, and its statistical relevance for the evidence. These results advance current literature in the philosophy and psychology of explanation in three ways. First, they yield a more nuanced understanding of the determinants of judgments of explanatory power, and the interaction between these factors. Second, they illuminate the close relationship between prior beliefs and explanatory power. Third, they clarify the relationship between abductive and probabilistic reasoning. (shrink)

In a very short time, it is likely that we will identify many of the genetic variants underlying individual differences in intelligence. We should be prepared for the possibility that these variants are not distributed identically among all geographic populations, and that this explains some of the phenotypic differences in measured intelligence among groups. However, some philosophers and scientists believe that we should refrain from conducting research that might demonstrate the (partly) genetic origin of group differences in IQ. Many scholars (...) view academic interest in this topic as inherently morally suspect or even racist. The majority of philosophers and social scientists take it for granted that all population differences in intelligence are due to environmental factors. The present paper argues that the widespread practice of ignoring or rejecting research on intelligence differences can have unintended negative consequences. Social policies predicated on environmentalist theories of group differences may fail to achieve their aims. Large swaths of academic work in both the humanities and social sciences assume the truth of environmentalism and are vulnerable to being undermined. We have failed to work through the moral implications of group differences to prepare for the possibility that they will be shown to exist. (shrink)

Molinists hold that there are contingently true counterfactuals about what agents would do if put in specific circumstances, that God knows these prior to creation, and that God uses this knowledge in choosing how to create. In this essay we critique Molinism, arguing that if these theses were true, agents would not be free. Consider Eve’s sinning upon being tempted by a serpent. We argue that if Molinism is true, then there is some set of facts that fully explains both (...) Eve’s action and everything else Eve does that influences that action; and that if this is the case, Eve does not act freely. The first premise of this argument follows from the explanatory relations the Molinist is committed to, and the second premise follows from libertarian intuitions about free will. (shrink)

"Correlation is not causation" is one of the mantras of the sciences—a cautionary warning especially to fields like epidemiology and pharmacology where the seduction of compelling correlations naturally leads to causal hypotheses. The standard view from the epistemology of causation is that to tell whether one correlated variable is causing the other, one needs to intervene on the system—the best sort of intervention being a trial that is both randomized and controlled. In this paper, we argue that some purely correlational (...) data contains information that allows us to draw causal inferences: statistical noise. Methods for extracting causal knowledge from noise provide us with an alternative to randomized controlled trials that allows us to reach causal conclusions from purely correlational data. (shrink)

When evaluating theories of causation, intuitions should not play a decisive role, not even intuitions in flawlessly-designed thought experiments. Indeed, no coherent theory of causation can respect the typical person’s intuitions in redundancy (pre-emption) thought experiments, without disrespecting their intuitions in threat-and-saviour (switching/short-circuit) thought experiments. I provide a deductively sound argument for these claims. Amazingly, this argument assumes absolutely nothing about the nature of causation. I also provide a second argument, whose conclusion is even stronger: the typical person’s causal intuitions (...) are thoroughly unreliable. This argument proceeds by raising the neglected question: in what respects is information about intermediate and enabling variables relevant to reliable causal judgment? (shrink)

The theory-theory of human uniqueness posits that the capacity to theorize, in a way strongly analogous to theorizing in scientific practice, was a key innovation in the hominid lineage and was responsible for many of our unique cognitive traits. One of the central arguments that its proponents have used to support the claim that animals are not theorists, the logical problem, bears strong similarities to Hempel's theoretician's dilemma, which purports to show that theories are unnecessary. This similarity threatens to undermine (...) both the claim that theorizing serves a unique, adaptive role in human cognition and our ability to test for the presence of theories. I examine two historical responses to the theoretician's dilemma and argue that they open up strategies for experimentally testing for theoretical ability in other animals. (shrink)

Current philosophical accounts of causation suggest that the same causal assertion can have different meanings. Yet, in actual social-scientific practice, the possible meanings of some causal generalisations intended to support policy prescriptions are not always spelled out. In line with a standard referentialist approach to semantics, we propose and elaborate on four questions to systematically elucidate the meaning of causal generalisations. The analysis can be useful to a host of agents, including social scientists, policy-makers, and philosophers aiming at being socially (...) relevant. To illustrate our proposal, we analyse the complexities related to the meaning of causal generalisations in the context of a concrete case of economic research which is explicitly intended to guide public policy, namely, the OECD research on the causes of unemployment. (shrink)

Mechanistic philosophy of science views a large part of scientific activity as engaged in modelling mechanisms. While science textbooks tend to offer qualitative models of mechanisms, there is increasing demand for models from which one can draw quantitative predictions and explanations. Casini et al. (Theoria 26(1):5–33, 2011) put forward the Recursive Bayesian Networks (RBN) formalism as well suited to this end. The RBN formalism is an extension of the standard Bayesian net formalism, an extension that allows for modelling the hierarchical (...) nature of mechanisms. Like the standard Bayesian net formalism, it models causal relationships using directed acyclic graphs. Given this appeal to acyclicity, causal cycles pose a prima facie problem for the RBN approach. This paper argues that the problem is a significant one given the ubiquity of causal cycles in mechanisms, but that the problem can be solved by combining two sorts of solution strategy in a judicious way. (shrink)

The most common way of analysing the meaning of causal generalisations relies on referentialist semantics. In this article, we instead develop an analysis based on inferentialist semantics. According to this approach, the meaning of a causal generalisation is constituted by the web of inferential connections in which the generalisation participates. We distinguish and discuss five classes of inferential connections that constitute the meaning of causal generalisations produced in policy-oriented economic research. The usefulness of our account is illustrated with the analysis (...) of generalisations about unemployment put forward by the Organisation for Economic Co-operation and Development in its highly influential 1994 OECD Jobs Study. The article ends with a discussion of some crucial philosophical questions about the use of inferentialism in the analysis of causal generalisations. (shrink)

Based on a crowdsourced truth value judgment experiment, we provide empirical evidence challenging two classical views in semantics, and we develop a novel account of counterfactuals that combines ideas from inquisitive semantics and causal reasoning. First, we show that two truth-conditionally equivalent clauses can make different semantic contributions when embedded in a counterfactual antecedent. Assuming compositionality, this means that the meaning of these clauses is not fully determined by their truth conditions. This finding has a clear explanation in inquisitive semantics: (...) truth-conditionally equivalent clauses may be associated with different propositional alternatives, each of which counts as a separate counterfactual assumption. Second, we show that our results contradict the common idea that the interpretation of a counterfactual involves minimizing change with respect to the actual state of affairs. We propose to replace the idea of minimal change by a distinction between foreground and background for a given counterfactual assumption: the background is held fixed in the counterfactual situation, while the foreground can be varied without any minimality constraint. (shrink)

Causal reasoning is an aspect of learning, reasoning, and decision-making that involves the cognitive ability to discover relationships between causal relata, learn and understand these causal relationships, and make use of this causal knowledge in prediction, explanation, decision-making, and reasoning in terms of counterfactuals. Can we fully automate causal reasoning? One might feel inclined, on the basis of certain groundbreaking advances in causal epistemology, to reply in the affirmative. The aim of this paper is to demonstrate that one still has (...) good skeptical grounds for resisting any conclusions in favour of the automation of causal reasoning. If by causal reasoning is meant the entirety of the process through which we discover causal relationships and make use of this knowledge in prediction, explanation, decision-making, and reasoning in terms of counterfactuals, then one relies besides on tacit knowledge, as might be constituted by or derived from the epistemic faculty virtues and abilities of the causal reasoner, the value systems and character traits of the causal reasoner, the implicit knowledge base available to the causal reasoner, and the habits that sustain our causal reasoning practices. While certain aspects of causal reasoning may be axiomatized and formalized and algorithms may be implemented to approximate causal reasoning, one has to remain skeptical about whether causal reasoning may be fully automated. This demonstration will involve an engagement with Meno’s Paradox. (shrink)

In this paper, two central questions will be addressed: ought we to implement medical AI technology in the medical domain? If yes, how ought we to implement this technology? I will critically engage with three options that exist with respect to these central questions: the Neo-Luddite option, the Assistive option, and the Substitutive option. I will first address key objections on behalf of the Neo-Luddite option: the Objection from Bias, the Objection from Artificial Autonomy, the Objection from Status Quo, and (...) the Objection from Inscrutability. I will thereafter present the Demographic Trends Argument and the Human Enhancement Argument in support of alternatives to the Neo-Luddite option. In the second half of the paper, I will argue against the Substitutive option and in favour of the Assistive option, given the existence of two chief formal deficits in medical AI technology: the causality deficit and the care deficit. (shrink)

Cognitive Science, Volume 46, Issue 5, May 2022.

Remarkable progress in the mathematics and computer science of probability has led to a revolution in the scope of probabilistic models. In particular, ‘sophisticated’ probabilistic methods apply to structured relational systems such as graphs and grammars, of immediate relevance to the cognitive sciences. This Special Issue outlines progress in this rapidly developing field, which provides a potentially unifying perspective across a wide range of domains and levels of explanation. Here, we introduce the historical and conceptual foundations of the approach, explore (...) how the approach relates to studies of explicit probabilistic reasoning, and give a brief overview of the field as it stands today. (shrink)

Judea Pearl has argued that counterfactuals and causality are central to intelligence, whether natural or artificial, and has helped create a rich mathematical and computational framework for formally analyzing causality. Here, we draw out connections between these notions and various current issues in cognitive science, including the nature of mental “programs” and mental representation. We argue that programs (consisting of algorithms and data structures) have a causal (counterfactual-supporting) structure; these counterfactuals can reveal the nature of mental representations. Programs can also (...) provide a causal model of the external world. Such models are, we suggest, ubiquitous in perception, cognition, and language processing. (shrink)

In this paper I argue that the Integrated Information Theory of Consciousness has an underlying emergentist metaphysics, specifically of a kind that has received minimal attention and we may call functionalist emergentism. I will try to show that in this scientific theory conscious experience is a functional-role property possessed by the whole system, not by their parts, which is dependent on, but also (purportedly) causally powerful over and above, the properties of the parts. However, I will argue that depicting conscious (...) experience as a functional-role emergent property threatens the whole coherence of the theory because, by definition, functional-realizers do all the causal work associated with the instantiation of any functional-role property on any occasion. Hence, to preserve the causal power of consciousness, which, as we will see, is one of the fundamental building blocks of the theory, linked to the assertion of the very existence of consciousness, phenomenal properties should be re-thought as realizers of the relevant informationally integrated causal-roles. (shrink)

The Recursive Bayesian Net formalism was originally developed for modelling nested causal relationships. In this paper we argue that the formalism can also be applied to modelling the hierarchical structure of mechanisms. The resulting network contains quantitative information about probabilities, as well as qualitative information about mechanistic structure and causal relations. Since information about probabilities, mechanisms and causal relations is vital for prediction, explanation and control respectively, an RBN can be applied to all these tasks. We show in particular how (...) a simple two-level RBN can be used to model a mechanism in cancer science. The higher level of our model contains variables at the clinical level, while the lower level maps the structure of the cell's mechanism for apoptosis. (shrink)

Mechanisms are usually viewed as inherently hierarchical, with lower levels of a mechanism influencing, and decomposing, its higher-level behaviour. In order to adequately draw quantitative predictions from a model of a mechanism, the model needs to capture this hierarchical aspect. The recursive Bayesian network formalism was put forward as a means to model mechanistic hierarchies by decomposing variables. The proposal was recently criticized by Gebharter and Gebharter and Kaiser, who instead propose to decompose arrows. In this paper, I defend the (...) RBN account from the criticism and argue that it offers a better representation of mechanistic hierarchies than the rival account. (shrink)

Glennan appeals to interventions to solve the ontological and explanatory regresses that threaten his mechanistic account of causality . I argue that Glennan’s manoeuvre fails. The appeal to interventions is not able to address the ontological regress, and it blocks the explanatory regress only at the cost of making the account inapplicable to non-modular mechanisms. I offer a solution to the explanatory regress that makes use of dynamic Bayesian networks. My argument is illustrated by a case study from systems biology, (...) namely, the mechanism for the irreversibility of apoptosis. I conclude by pointing out the implications of my argument for Glennan’s mechanistic account of causality and, more generally, for accounts of mechanistic explanation based on interventions. 1 Introduction2 Glennan’s Account of Causality3 Objections to Glennan’s Account4 Glennan’s Replies5 Ontological Symmetry?6 Explanatory Symmetry?7 A Solution to the Explanatory Regress8 The Prospects of Glennan’s Account. (shrink)

Randomized controlled trials (RCTs) are widely taken as the gold standard for establishing causal conclusions. Ideally conducted they ensure that the treatment ‘causes’ the outcome—in the experiment. But where else? This is the venerable question of external validity. I point out that the question comes in two importantly different forms: Is the specific causal conclusion warranted by the experiment true in a target situation? What will be the result of implementing the treatment there? This paper explains how the probabilistic theory (...) of causality implies that RCTs can establish causal conclusions and thereby provides an account of what exactly that causal conclusion is. Clarifying the exact form of the conclusion shows just what is necessary for it to hold in a new setting and also how much more is needed to see what the actual outcome would be there were the treatment implemented. (shrink)

In much recent work, invariance under intervention has become a hallmark of the correctness of a causal-law claim. Despite its importance this thesis generally is either simply assumed or is supported by very general arguments with heavy reliance on examples, and crucial notions involved are characterized only loosely. Yet for both philosophical analysis and practicing science, it is important to get clear about whether invariance under intervention is or is not necessary or sufficient for which kinds of causal claims. Furthermore, (...) we need to know what counts as an intervention and what invariance is. In this paper I offer explicit definitions of two different kinds for the notions intervention, invariance, and causal correctness. Then, given some natural and relatively uncontroversial assumptions, I prove two distinct sets of theorems showing that invariance is indeed a mark of causality when the concepts are appropriately interpreted. (shrink)

There is danger in stressing commonalities among methods because the differences matter in fixing the meaning of our claims. Different methods can, and often do, test the same claim. But it takes a strong network of theory and empirical results to ensure that. Failing that, we are likely to fall into inference by pun. We use one set of methods to establish a claim and then draw inferences licensed by a similar-sounding claim that calls for different methods of testing. Our (...) inferences fail, and bridges we build depending on them fall down. (shrink)

We currently have on offer a variety of different theories of causation. Many are strikingly good, providing detailed and plausible treatments of exemplary cases; and all suffer from clear counterexamples. I argue that, contra Hume and Kant, this is because causation is not a single, monolithic concept. There are different kinds of causal relations imbedded in different kinds of systems, readily described using thick causal concepts. Our causal theories pick out important and useful structures that fit some familiar cases—cases we (...) discover and ones we devise to fit. (shrink)

An alleged counterexample to causal decision theory, put forward by Andy Egan, is studied in some detail. It is argued that Egan rejects the evaluation of causal decision theory on the basis of a description of the decision situation that is different from—indeed inconsistent with—the description on which causal decision theory makes its evaluation. So the example is not a counterexample to causal decision theory. Nevertheless, the example shows that causal decision theory can recommend unratifiable acts which presents a problem (...) in the dynamics of intentions. It is argued that we can defuse this problem if we hold that decision theory is a theory of rational decision making rather than a theory of rational acts. It is shown how decisions can have epistemic side-effects that are not mediated by the act and that there are cases where one can only bring oneself to perform the best act by updating by imaging rather than by conditioning. This provides a pragmatic argument for updating by imaging rather than by conditioning in these cases. (shrink)

In this paper, we investigate the semantics and logic of choice-driven counterfactuals, that is, of counterfactuals whose evaluation relies on auxiliary premises about how agents are expected to act, i.e., about their default choice behavior. To do this, we merge one of the most prominent logics of agency in the philosophical literature, namely stit logic, with the well-known logic of counterfactuals due to Stalnaker and Lewis. A key component of our semantics for counterfactuals is to distinguish between deviant and non-deviant (...) actions at a moment, where an action available to an agent at a moment is deviant when its performance does not agree with the agent’s default choice behavior at that moment. After developing and axiomatizing a stit logic with action types, instants, and deviant actions, we study the philosophical implications and logical properties of two candidate semantics for choice-driven counterfactuals, one called rewind models inspired by Lewis, 455–476 1979) and the other called independence models motivated by well-known counterexamples to Lewis’s proposal Slote, 3–27 1978). In the last part of the paper we consider how to evaluate choice-driven counterfactuals at moments arrived at by some agents performing a deviant action. (shrink)

Recently, it has been argued that the use of Big Data transforms the sciences, making data-driven research possible and studying causality redundant. In this paper, I focus on the claim on causal knowledge by examining the Big Data project EXPOsOMICS, whose research is funded by the European Commission and considered capable of improving our understanding of the relation between exposure and disease. While EXPOsOMICS may seem the perfect exemplification of the data-driven view, I show how causal knowledge is necessary for (...) the project, both as a source for handling complexity and as an output for meeting the project’s goals. Consequently, I argue that data-driven claims about causality are fundamentally flawed and causal knowledge should be considered a necessary aspect of Big Data science. In addition, I present the consequences of this result on other data-driven claims, concerning the role of theoretical considerations. I argue that the importance of causal knowledge and other kinds of theoretical engagement in EXPOsOMICS undermine theory-free accounts and suggest alternative ways of framing science based on Big Data. (shrink)

The Central Dogma of molecular biology, which holds that DNA makes protein and not the other way around, is as influential as it is controversial. Some believe the Dogma has outlived its usefulness, either because it fails to fully capture the ins-and-outs of protein synthesis (Griffiths and Stotz, 2013; Stotz, 2006), because it turns on a confused notion of information (Sarkar, 2004), or because it problematically assumes the unidirectional flow of information from DNA to protein (Gottlieb, 2001). This paper evaluates (...) an underexplored defense of the Dogma, which relies on the assumption that the Dogma and the Inheritance of Acquired Traits, a principle which dates as far back as Jean Baptiste-Lamarck, are incompatible principles (Smith, 1993; Judson, 1979; Dawkins, 1970; Cobb, 2017; Wilkins, 2002; Graur, 2018). By appealing to empirical evidence in molecular science, I argue that this apparent incompatibility is indeed merely apparent. I conclude by briefly demonstrating how these considerations bear on the topic of conceptual pluralism in the philosophy of science (Stencel and Proszewska, 2018; Lu and Bourrat, 2018). (shrink)

The purpose of this article is to examine two important issues concerning the agency theory of causality: the charge of anthropomorphism and the relation of simultaneous causation. After a brief outline of the agency theory, sections 2–4 contain the refutation of the three main forms in which the charge of anthropomorphism is to be found in the literature. It will appear that it is necessary to distinguish between the subjective and the objective aspect of the concept of causation. This will (...) lead, in section 5, to contrast two kinds of anthropomorphism, one which has been rightly rejected by modern science and one which is fully compatible with the objective reality of the causal processes. Finally, section 6 will apply the preceding considerations to simultaneous causation. On the one hand, in a basic sense, there can be no simultaneous causal relations. On the other hand, simultaneous causation arises when we consider the natural change by abstracting from the agent and from her/his projects of interven.. (shrink)

Users of sociotechnical systems often have no way to independently verify whether the system output which they use to make decisions is correct; they are epistemically dependent on the system. We argue that this leads to problems when the system is wrong, namely to bad decisions and violations of the norm of practical reasoning. To prevent this from occurring we suggest the implementation of defeaters: information that a system is unreliable in a specific case (undercutting defeat) or independent information that (...) the output is wrong (rebutting defeat). Practically, we suggest to design defeaters based on the different ways in which a system might produce erroneous outputs, and analyse this suggestion with a case study of the risk classification algorithm used by the Dutch tax agency. (shrink)

According to a prominent claim in recent epistemology, people are less likely to ascribe knowledge to a high stakes subject for whom the practical consequences of error are severe, than to a low stakes subject for whom the practical consequences of error are slight. We offer an opinionated "state of the art" on experimental research about the role of stakes in knowledge judgments. We draw on a first wave of empirical studies--due to Feltz & Zarpentine (2010), May et al (2010), (...) and Buckwalter (2010)--which cast doubt on folk stakes sensitivity, and a second wave of empirical studies--due to Pinillos (2012) and Sripada & Stanley (2012)--said to vindicate it, as well as new studies of our own. We conclude that the balance of evidence to date best supports Folk stakes insensitivity, or that all else equal, stakes do not affect knowledge ascription. (shrink)

Philosophers have recently highlighted substantial affinities between causation and grounding, which has inclined some to import the conceptual and formal resources of causal interventionism into the metaphysics of grounding. The prospect of grounding interventionism raises two important questions: exactly what are grounding interventions, and why should we think they enable knowledge of grounding? This paper will approach these questions by examining how causal interventionists have addressed (or might address) analogous questions and then comparing the available options for grounding interventionism. I (...) argue that grounding interventions must be understood in worldly terms, as adding something to or deleting something from the roster of entities, or making some fact obtain or fail to obtain. I consider three bases for counterfactual assessment: imagination, structural equation models, and background theory. I conclude that grounding interventionism requires firmer epistemological foundations, without which the interventionist's epistemology of grounding is incomplete and ineffectually rationalist. (shrink)

In recent years, pragmatism in general and John Dewey in particular have been of increasing interest to philosophers of science. Dewey's work provides an interesting alternative package of views to those which derive from the logical empiricists and their critics, on problems of both traditional and more recent vintage. Dewey's work ought to be of special interest to recent philosophers of science committed to the program of analyzing ``science in practice.'' The core of Dewey's philosophy of science is his theory (...) of inquiry---what he called ``logic.'' There is a major lacuna in the literature on this point, however: no contemporary philosophers of science have engaged with Dewey's logical theory, and scholars of Dewey's logic have rarely made connections with philosophy of science. This paper aims to fill this gap, to correct some significant errors in the interpretation of key ideas in Dewey's logical theory, and to show how Dewey's logic provides resources for a philosophy of science. (shrink)

When is a cause of a cause of an effect also a cause of that effect? The right answer is either Sometimes or Always . In favour of Always , transitivity is considered by some to be necessary for distinguishing causes from redundant non-causal events. Moreover transitivity may be motivated by an interest in an unselective notion of causation, untroubled by principles of invidious discrimination. And causal relations appear to add up like transitive relations, so that the obtaining of the (...) overarching relation is not independent of the obtaining of the intermediaries. On the other hand, in favour of Sometimes , often we seem not to treat events that are very spatiotemporally remote from an effect as its causes, even when connected to the effect in question by a chain of counterfactual or chance-raising dependence. Moreover cases of double prevention provide counterexamples to causal transitivity even over short chains. According to the argument of this paper, causation is non-transitive. Transitizing causation provides no viable account of causal redundancy. An unselective approach to causation may motivate resisting the distance counterexamples to transitivity, but it does not help with double prevention, and even makes it more intractable. The strongest point in favour of transitivity is the adding up of causal relations, and this is the point that extant non-transitizing analyses have not adequately addressed. I propose a necessary condition on causation that explains the adding up phenomenon. In doing so it also provides a unifying explanation of distance and double prevention counterexamples to transitivity. (shrink)

Contributing to the recent debate on whether or not explanations ought to be differentiated from arguments, this article argues that the distinction matters to science education. I articulate the distinction in terms of explanations and arguments having to meet different standards of adequacy. Standards of explanatory adequacy are important because they correspond to what counts as a good explanation in a science classroom, whereas a focus on evidence-based argumentation can obscure such standards of what makes an explanation explanatory. I provide (...) further reasons for the relevance of not conflating explanations with arguments (and having standards of explanatory adequacy in view). First, what guides the adoption of the particular standards of explanatory adequacy that are relevant in a scientific case is the explanatory aim pursued in this context. Apart from explanatory aims being an important aspect of the nature of science, including explanatory aims in classroom instruction also promotes students seeing explanations as more than facts, and engages them in developing explanations as responses to interesting explanatory problems. Second, it is of relevance to science curricula that science aims at intervening in natural processes, not only for technological applications, but also as part of experimental discovery. Not any argument enables intervention in nature, as successful intervention specifically presupposes causal explanations. Students can fruitfully explore in the classroom how an explanatory account suggests different options for intervention. (shrink)

A number of recent authors (Galles and Pearl, Found Sci 3 (1):151–182, 1998; Hiddleston, Noûs 39 (4):232–257, 2005; Halpern, J Artif Intell Res 12:317–337, 2000) advocate a causal modeling semantics for counterfactuals. But the precise logical significance of the causal modeling semantics remains murky. Particularly important, yet particularly under-explored, is its relationship to the similarity-based semantics for counterfactuals developed by Lewis (Counterfactuals. Harvard University Press, 1973b). The causal modeling semantics is both an account of the truth conditions of counterfactuals, and (...) an account of which inferences involving counterfactuals are valid. As an account of truth conditions, it is incomplete. While Lewis's similarity semantics lets us evaluate counterfactuals with arbitrarily complex antecedents and consequents, the causal modeling semantics makes it hard to ascertain the truth conditions of all but a highly restricted class of counterfactuals. I explain how to extend the causal modeling language to encompass a wider range of sentences, and provide a sound and complete axiomatization for the extended language. Extending the truth conditions for counterfactuals has serious consequences concerning valid inference. The extended language is unlike any logic of Lewis's: modus ponens is invalid, and classical logical equivalents cannot be freely substituted in the antecedents of conditionals. (shrink)

Identifying causal relations from correlational data is a fundamental challenge in personality psychology. In most cases, random assignment is not feasible, leaving observational studies as the primary methodological tool. Here, we document several techniques from behavior genetics that attempt to demonstrate causality. Although no one method is conclusive at ruling out all possible confounds, combining techniques can triangulate on causal relations. Behavior genetic tools leverage information gained by sampling pairs of individuals with assumed genetic and environmental relatedness or by measuring (...) genetic variants in unrelated individuals. These designs can find evidence consistent with causality, while simultaneously providing strong controls against common confounds. We conclude by discussing several potential problems that may limit the utility of these techniques when applied to personality. Ultimately, genetically informative designs can aid in drawing causal conclusions from correlational studies. (shrink)